Cardiovascular System Flashcards
The information from this deck should be pulled from: Netter's Physiology USMLE Review Book BRE review Book Lecture MNTS from 2016
Pulmonary hypertension
Right ventricular hypertrophy occurs in response to heightened pressure in the lungs
Aortic stenosis
Narrowing of the aortic valve that results in left ventricle hypertrophy
Mitral incompetence
Left atrial dilation may develop as a result of the elevation of left atrial pressure and volume caused by mitral regurgitation
What is the pulmonary arterial pressure?
25/10 (mean pressure 15)
What aortic pressure?
120/80 (mean pressure 95)
What is the volume distribution in the blood of the body?
64% veins 9% lungs 8% small arteries & arterioles 7% large arteries 7% heart in diastole 5% capillaries
What is the distribution of vascular resistance?
47% arterioles 27% capillaries 19% large arteries 7% veins
What is the distribution of blood flow in the body?
24% liver and GI 21% skeletal muscle 20% kidney 18% skin and other organs 13% brain 4% heart
What is VO2 distribution of blood flow in the body?
27% skeletal 23% liver and GI 21% brain 11% skin and other organs 11% heart 7% kidney
What is the resting membrane potential of the SA node?
-60mV
What is a normal rate of the SA node?
70 bpm
What are the phases of the action potentials of myocytes and His-Purkinje fiber?
Phase 4 (resting membrane potential): Close to the Nernst potential for K because of the efflux of K. Ion levels are restored by the Na/K pump, the Na/Ca exchanger, and the ATP-dependent Ca pump. Phase 0 (upstroke of the action potential): When cells reach threshold, Na ion gated channels open coupled with reduced conductance of K current. This depolarizes the cell. Phase 1 (rapid repolarization to the plateau): Na channel are inactivated and voltage gated K channels are opened. Phase 2 (the plateau): Slow L type Ca channels and inward current of Ca moderates the effects of the outflow of K. Phase 3 (repolarization): Gradual inactivation of the L-type Ca channels leads to activation of K channels causing rapid depolarization.
Effective refractory period
Phase 1 to much of phase 3, during which an AP cannot be generated
Relative refractory period
Until membrane potential is restored, an AP can be generated but it is more difficult
Chronotropic
effects heart rate
Dromotropic
effects conduction velocity
Inotropic
effects myocardial contractility
What effect does the sympathetic nervous system have on chromotoropic, dromotropic, and inotropics?
Increases them
What effect does the parasympathetic nervous system have on chromotoropic, dromotropic, and inotropics
Decreases them
P wave
atrial depolarization
QRS complex
ventricular depolarization
T wave
ventricular repolarization
Bradycardia
resting heart rate below 60 bpm
Tachycardia
resting heart rate above 100 bpm
First degree AV block
Delay in conduction through the AV node. Thus, there is an extended PR interval with normal sinus rhythm.
Normal PR interval
0.20 s
Second degree AV block
Delay in conduction through the AV node that sometimes does not result in a QRS complex. This may be produced by ischemia or infarction.
Third degree AV block
Complete blockage of the AV node. P waves are dissociated from the QRS complexes with an escape pacemaker below the AV node with a rate of 40-55 bpm which is partially responsive to the sympathetics. When the block is below in the bundle of His, the escape rhythm is 20-40 bpm which can be insufficient even at rest. Usually a pacemaker is put in at this point.
Describe action potential of pacemaker cells (SA node cells)
ADD INFO!
Describe the pathway of the electrical charge through the heart.
SA node –> AV node –> bundle of his –> bundle branchs fiber –> Purkinje fibers –> ventricular muscle
U wave
Occurs in 50-70% of people following the T wave.
Equation for rate of flow
Q = change in pressure/resistance Q = P/R
Systolic arterial pressure
peak arterial pressure reached at point of ejective of blood by heart, usually 120
Diastolic arterial pressure
lowest arterial pressure reached during diastole, usually 80
Arterial pulse pressure
Systolic pressure - diastolic pressure depends on the stroke volume
Mean arterial pressure
average pressure over a complete cardiac cycle of systole and diastole dependent on peripheral resistance and cardiac output MAP = 1/3(pulse pressure) + diastolic pressure
NB: Pulse pressure is the difference between diastolic and systolic pressure
What factors impact arterial pressure?
arterial compliance, cardiac output, stroke volume, peripheral resistance
Dichrotic notch
irregular notch in the descending slop of the arterial pressure curve representing when the aortic valves close
Pressure right ventricle
25/0
Pressure left ventricle
125/0
Poiseuille’s law
Q = P(pi)r^4/n8L (n = viscosity) Flow is… directly: pressure gradient, radius indirectly: viscosity, length
What is the most important factor that influences flow?
The radius of the tube because that value is raised to the fourth power.
Sounds of Korotkoff
pulsatile sounds heard during blood pressure readings
Pulmonary capillary wedge pressure
Venous catheter is passed from veins, right atrium, and right ventricles. We cannot measure the pulmonary venous pressure directly nor the left atria pressure, so the wedge pressure is used. Swan-Gatz catheters have an inflated balloon at the end. Vascular pressure beyond the occlusion equilibrates with downstream pressure and wedge pressure is an indicator of pulmonary venous pressure and left atrial pressure.
Left atrial pressure
15/0
Contrast pulse pressures throughout the body.
Left atria: 15 Left ventricle: 125 Aorta: 40 Large arteries: 60 Capillaries & veins: 0 Right atrium: 5 Right ventricle: 25
Right ventricle pressure
25/0
Resistance equation
R = n8L/(pi)r^4 directly: length, viscosity indirectly: radius
Flow equation
Q = VA
Laminar flow
greatest velocity of flow in the center of the vessel, R below 2000
Reynold’s Number (R)
R = VDd/n V = velocity D = diameter d = density n = viscosity
Turbulent flow
Flow promoted by high velocity of blood flow, large vessel diameter, low viscosity of blood, abrupt changes in vessel diameter, and vascular branching points; R above 3000; associated with murmurs
Wall tension
force necessary to hold together a slit in a vessel’s wall
Leplace’s law
T = Pr P = intramural pressure, difference between pressure inside and outside the vessel r = radius
Aortic aneurysm
Enlargement of the aorta caused by a weakness in the aorta.
Left heart valves sequence
Mitral closure, aortic opening, aortic closing, mitral opening
Right heart valves sequence
Tricuspid closure, pulmonic opening, pulmonic closure, tricuspid opening
Aggregate sequence of valves
Mitral valve closure, tricuspid closure, pulmonic opening, aortic opening, aortic closure, pulmonic closure, tricuspid opening, mitral opening
What causes the asynchrony between the right and left valves?
Pressure gradient between the sides of circulation.
Cardiac output
CO = HR x SV normally 5L/min
Cardiac Cycle/ Wiggers Diagram
One cycle of ventricular diastole and systole (Map out image)
isovolumetric contraction
The period during systole when all the valves are shut
isovolumetric relaxation
The period during diastole when all the valves are shut
dicrotic notch
A high frequency deflection in the aortic pressure curve when the aortic valve closes
Describe the timing of filling the ventricles?
By the time of the P wave, most of the blood has filled the ventricles, but the remaining 15% is pushed in with the contraction of the atria.
Active ventricular filling
The 15% of blood that is pushed into the ventricles by the atrial contraction
End diastolic volume (EDV)
The volume at the end of diastole with the closure of the mitral valve. (Normal 140 mL)
End systolic volume (ESV)
The volume at the end of systole with the closure of the aortic valve.
Stroke volume
EDV - ESV (Normal 70 mL)
Rapid passive filling
Opening of the mitral valve leads to filling of the ventricles.
Slow passive feeling (diastasis)
Ventricle fills more slowly because of different pressure differential.
A wave
Atrial contraction makes this wave
C wave
During isovolumetric contraction, there is an upward wave in the LAP curve
V wave
During ejection phase, LAP rises with venous return to the atrium (during mitral valve closure)
Why are the venous pulse and the atrial pulse similar?
Because there are no valves between the vena cave and right atrium, the atrial pressure curve and venous pulse are similar in shape
Phonocardiogram
acoustical recording reflecting the heart sounds generated during the cardiac cycle
S1
closure of mitral and tricuspid valves
S2
closure of aortic and pulmonic valves
What happens during inspiration to S2?
During S2, there is a delay causing more filling in the right ventricle due to decreased intrathoracic pressure.
S3
normal in children, associated with rapid ventricle filling; not heard in normal adults and is a sign of volume overload in congestive heart failure
S4
active ventricular filling not heard in normal adults
How does the autonomic nervous system play a role in regulating cardiac output?
The ANS modulates the SA nodal pacemaker rate, myocardial contractility, and vascular smooth muscle tone. Sympathetics - release catecholamines to vessels and heart and a few vascular beds. There is some circulating epinephrine from the adrenal glands as well. Parasympathetics - release Ach to heart and some vascular beds.
How is cardiac input regulated in response to a change in posture (standing to lying down)?
Increase in venous return –> Increase stroke volume –> increase MAP –> Increase rate of baroreceptor afferent fibers –> increase PNS activity acting on SA node to reduce heart rate and CO –> decrease MAP Increase in venous return –> Increase stroke volume –> increase MAP –> Increase rate of baroreceptor afferent fibers –> decrease sympathetics –> decrease peripheral resistance, decrease venous tones, decrease contractility (decrease stroke volume) –> lower cardiac output –> decrease MAP
What mechanisms regulate heart rate?
ANS - sympathetics B1 receptor increases cAMP production raising pacemaker and elevation of heart rate; parasympathetics reduce heart rate with Ach Bainbridge reflex response to atrial stretch Thoracic pressure changes during respiration on venous return
Respiratory sinus arrythmia
Heart rate is increased with inspiration and decreased with expiration.
Bainbridge reflex
Low-pressure stretch receptors in the atria initiate reflex that increases heart rate through sympathetic nerves
Contrast the effects of arterial baroreceptors and atrial baroreceptors.
Arterial baroreceptors is a response to regulate arterial pressure and reduces heart rate. Atrial baroreceptors is a response to increase blood volume and increases heart rate.
Describe how intravenous infusion can either cause an increased or decreased heart rate depending on the circumstances.
When the subject initially had a slow heart rate, with the infusion the Bainbridge reflex will take over and increase the heart rate. However, if the subject had experienced a hemorrhage and had an elevated heart rate, the infusion would result in a decreased heart rate.
What parameters is stroke volume dependent on?
Preload, afterload, contractility
Preload
Degree of stretch of myocardial fibers prior to contraction; correlates with EDV; directly related to stroke volume
Afterload
Force against which the heart has to pump; correlates with arterial pressure or left ventricular pressure during systole; inversely related to stroke volume
Contractility (inotropism)
Intrinsic ability of cardiac muscle to generate a force at a given fiber length; NOT the same as the force of contraction
Frank-Starling relationship
An important mechanism for matching cardiac output and venous return and ride and left side cardiac output. An increase in the preload results in an increase in stroke volume and cardiac output. When under sympathetic stimulation, the curve is shifted up and to the left. When under cardiac failure, it gives a lower slope of the curve. In this graph the afterload is assumed to be constant.
Cardiac function curve
LOOK THIS UP!
How does the sympathetic nervous system regulate the stroke volume?
Cardiac muscle is directly innervated with sympathetic nerves that release norepinephrine which binds to B1 receptors, increasing intracellular Ca, increasing contractility of the heart. This may also be caused by an increased release of epi by the adrenal medulla.
What drugs are used to promote contractility?
digitalis, dopamine, and dobutamine
Treppe OR Staircase Effect
When intervals between cardiac muscle contractions are long, the tension developed is low. There is a stair-like increase in the force of contraction hen frequency (heart rate) is increased. This is associated with an increase in contractility because it is independent from a change in preload. This is associated with higher free intracellular Ca in myocardial fibers.
In response to baroreceptor detected fall in arterial pressure, how does cardiac output change?
Sympathetics elevate the heart rate; however, this is not effective because the amount of time to fill the heart is smaller so the preload is smaller. By raising the contractility of the heart as well, sympathetics also increase stroke volume. Sympathetic constriction of the venous system elevates the preload of the heart as well.
force-velocity relationship
Inverse relationship between velocity and maximal contraction. Maximal contraction is when the velocity is 0. Velocity is highest at 0 afterload. Maximum force of contraction occurs at zero velocity, during an isometic contraction.
How will the force-velocity relationship change with an increase in preload?
Changes in preload result in a family of curves upshifted with the same y-intercept, the same Vm. Vm represents the maximal velocity and corresponds with contractility, so with no change in contractility, the Vm will stay the same. The curve shifts upwards because of the Frank-Starling relationship - greater preload results in greater force of contraction, thus velocity of contraction.
How will the force-velocity relationship change with an increase in contractility?
This curve will shift up and to the right, thus changing the Vm. Vm is associated with the contractility of the heart. An increased Vm is indicative of a positive ionotropic effect.
Ventricular pressure-volume loop
A continuous measurement of ventricular volume and ventricular pressure. LOOK THIS IMAGE UP! This can be changed with changes in contractility, preload, and afterload.
Ejection fraction
Normal >50%
What effect will a positive ionotropic drug on ejection fraction?
Increase
What effect would MI or heart failure have on ejection fraction?
Decrease
Echocardiogram
Sounds are used to produce an image of the heart.
How does an increase in stroke volume change a ventricular pressure-volume curve?
How does an increase in afterload influence pressure voume curves?
How does an increase in contractility change presssure volume curves?
What is normal venous return?
5L/min; normally it should balance out with cardiac output
Compliance
Change in volume associated with a change in pressure
Orthostatic hypotension
decreased blood pressure with standing
What is the impact of the baroreceptor reflex on the veins?
Constriction of the venous sytem in response to sympathetics prevents the pooling of blood in the extermities.
What is the effect of respiration on venous return?
During inspiration, the rib cage expands, negative pressure is created in the thorax, diaphragm creates positive pressure in abdomen augmenting return to the thorax
During expiration, the gradient is reduced
Vascular function curve
Cardiac output is an independent variable on the y-axis and the dependent variable of right atrial pressure is on the x axis.
This is an inverse relationship.
Mean circulatory pressure
X intercept of the vascular function curve; the pressure at which cardiac output is zero; pressure if the heart stopped beating at the whole blood volume equilibriated
Describe a normal curve integrating the vascular and cardiac function curves.
ADD IMAGE
Describe a normal curve integrating the vascular and cardiac function curves.
How does a change in volume cahnge vascular and cardiac function curves?
How does contractility change the vascular and cardiac function curves?
How does total peripheral resistance influence the vascular and cardiac function curves?
Note that MCP stays the same because the volume has remained constant.
Tunica intima
Innermost layer of endothelial cells; rest on a basement membrane that separates the intima from the media
Tunica media
Smooth muscle; contractile portion of the vessel
Tunica adventitia
consists of mainly connective tissue and is the outer layer of vessels
Contrast the layers of cells lining vessels for arteries, veins, and capillaries.
Arteries: Thick adventitia compared to small arteries (distributing vessels)
Small arteries: Larger media layers (needed for blood flow regulation)
Capillaries: No media or adventitia, single layer of endothelial cells (needed for diffusion)
Veins: circular and longitudinal adventitia (capicitance tubes)
Precapillary sphincters
Bands of smooth muscle found at the point at which arteries feed into capillaries. These can open and shut to regulate blood flow to capillary beds.
Edema
swelling with an increase in interstitial fluid
vasa vasora
Own vascular supply of arteries
internal and external elastic membranes
bind the tunica media of arteries
In general, how is blood flow regulated?
change in resistance, flow, or cardiac output
Describe how vasodilators act to regulate vascular tone of endothelial cells?
What are vasodilators?
nitrous oxide, prostacylcin
What factors stimulate the release of vasodilators?
Sheer stress, histamine, Ach, bradykinin, purigenics (ATP)
What is the chemical reaction of NO?
NO acts on guanalyn cyclase, elevating GMP, cGMP reduces free cellular Ca, reducing the tension of smooth muscle.
What opposes the actions of prostacylin?
Thromboxane A2
Endothelin
Vasoconstrictor
Angiotensin converting enzyme (ACE)
Found in endothelium cells, it converts ang I to ang II. Plays a role in water retention with ADH. Plays a role in long term water retention and acute response to hemorrage, but not moment to moment regulation.
Reactive hyperemia
When blood flow is reestablished after a temporary occlusion, blood flow is elevated above its original level. Local metabolites (CO2, H, K, lactic acid, and adenosine) accumulate and act to produce vasodilation until) O2 levels are restored.
Active hyperemia
Increase in flow beccause of increased metabolic needs of surrounding tissue.
Example: skeletal muscle during exercise
Transmural pressure
Difference in pressure between two walls
Example: in blood vessel and outside of the vessel
Myogenic hypothesis
Smooth muscle cells respond to changes in transmural pressure, stretch, by constricting. This keeps flow to a tissue fairly constant when the metabolic needs of the tissue are not changing.
Autoregulation
Changes in flow without changes in local metabolism. It is the intrinsic ability of the vessel to maintain constant blood flow without changes in perfusion pressure. This impacts the smooth muscle of the vessels.
What are methods of extrinsic regulation of blood flow?
vasodilation and vasoconstriction in response to neural signals
Alpha receptors
Constrictor response to catecholamines
Alpha 1: vessels, mediated by inositol triphosphate
Alpha 2: vasoconstrictors by means of reducing uptake of norepi, mediated by reduced cAMP levels
B2 receptors
dilator response to catetcholamines, mediated by cAMP
How do sympathetics affects vasodilation/constriction?
Sympathetic action depends on the concentration of receptor types in the region, but predominantly has the impact of constriction. This results in increased blood pressure because of increased vascular resistance in arteries. The veins are also constricted increasing preload on the heart. However, in areas like skeletal muscle, B2 concentration is higher and there is increased blood flow, resulting in readiness for “fight or flight” response.
Contrast the sympathetic and parasympathetic innervation of vessels.
Sympathetics are present almost all vessles and parasympathetic innervation is rare in vessels except genital organs, salivary glands, and lower GI.
What is the role of chemoreceptors in extrinsic regulation of vascular tone?
Response to the levels of O2 and CO2 to promote constriction or dilation when needed.
Ejection fraction
EJ = SV/EDV
Normally >55%
Relate cardiac output to oxygen consumption via equation
CO = oxygen consumption(ml/min)/(a-v)
